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논문 기본 정보

자료유형
학술저널
저자정보
Kim, Dong-Woon (Swine Science Division, National Institute of Animal Science, RDA) Cho, Sung-Back (Swine Science Division, National Institute of Animal Science, RDA) Jung, Hyun-Jung (Swine Science Division, National Institute of Animal Science, RDA) Lee, Sung-Dae (Swine Science Division, National Institute of Animal Science, RDA) Kim, Sang-Ho (Swine Science Division, National Institute of Animal Science, RDA) Cho, Kyu-Ho (Swine Science Division, National Institute of Animal Science, RDA) Kang, Seog-Jin (Swine Science Division, National Institute of Animal Science, RDA) Kim, In-Cheul (Swine Science Division, National Institute of Animal Science, RDA)
저널정보
한국축산식품학회 한국축산식품학회지 한국축산식품학회지 제30권 제5호
발행연도
2010.1
수록면
739 - 745 (7page)

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The objective of the current study was to compare the abilities of undigested and enzymatically digested bifidobacteria to induce nitric oxide and cytokine release in RAW 264.7 macrophage cells. Nine different Bifidobacterium strains derived from herbivorous animals were digested with pepsin and then pancreatin, and the precipitates and supernatants were acquired via centrifugation. The RAW 264.7 cells were incubated with whole cells, the precipitate, or the supernatant, and the macrophage culture supernatants were analyzed with respect to the induction of nitric oxide and cytokines. Pronounced increases in the production of nitric oxide, interleukin (IL)-$1{\beta}$, IL-6, IL-12, and tumor necrosis factor-$\alpha$ (TNF-$\alpha$) were observed when cultured with whole cells and the precipitates. It is noteworthy that the precipitates in most of the Bifidobacterium strains evidenced a trend toward superior IL-12 release compared with whole cells. The results showed that both whole cells and digested Bifidobacterium sp. are effective at stimulating RAW 264.7 cells to induce the production of nitric oxide and cytokines. The pepsin-pancreatin system used in the current study may be useful in unraveling the mechanism by which ingested lactic acid bacteria modulate the induction of macrophage mediators at the cellular level.

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